Dog Bite Wounds



Dog bite wounds are common and canine victims of dog bite wounds can constitute up to 10% of canine trauma admissions. This is especially significant in areas with poorly enforced or non-existent leash laws1. The trauma of a dog bite differs from other traumatic injuries:

1. The jaws of a large dog are capable of producing pressures that can severely bruise and crush tissue (150 to 450 psi of crushing force can be transmitted)2. Canine skin is freely movable, thus the cutaneous injury might not always reflect the extent of subcutaneous or visceral trauma1.

2. Bite wounds result in punctures, crushing injuries, lacerations, or avulsion of flaps of skin or other tissue. Some bite wounds only exhibit a small surface wound, but with great underlying tissue damage. The animal may show only a few puncture wounds with bloodied hair matted over them when brought in for examination, but there may be severe lacerations, punctured lungs, nerve damage, torn abdominal viscera, or fractures that are not readily detectable1. Hence the term "Iceberg" injury.

3. During the slashing action of a bite, the tooth moves through the underlying subcutaneous and muscular tissue, but the skin slides with the movement of the tooth3. The results are torn muscles, separated fascia planes, and/or severed tendons, blood vessels and nerves. This can result in a lot of devitalized tissue, avulsion of the skin from the underlying subcutaneous tissue, and damage to vital structures.

4. The wounds are inoculated with the attacker's oral microbial flora and, to a lesser degree, organisms found on the victim's hair coat. In some instances soil organisms may also be embedded into the bite wound4. The mechanically inoculated aerobic and anaerobic bacteria are often synergistically active, and thrive in the environment created by dead space, serum and blood accumulation, as well as devitalized tissue. No single antimicrobial agent has been demonstrated to be active against all of these different potential pathogens5. Bacteraemia is found in half of the patients with septic shock, and is most frequently caused by gram-negative bacteria, and the sources of infection include bite wounds, and/or perforation of the gastrointestinal or urogenital tracts6. Occasionally, the skin puncture wound heals, but the bacteria continue to grow in the deeper tissues, causing cellulitis or abscess formation with intermittent draining sinuses in the area3.

5. In extensively bitten individuals the attendant veterinarian should anticipate that these patients will often deteriorate a few days after injury due to the accumulated toxic effects of massive tissue necrosis and sepsis. The development of systemic inflammatory response syndrome (SIRS), the response of the body to the resultant cascade of inflammatory mediators and progression to frequently fatal multiple organ dysfunction syndrome (MODS) is well documented in severely traumatised\septic patients11. Prevention of the occurrence of these two life-threatening conditions is easier than treating a patient where they already have occurred. Animals presented with multiple puncture wounds or crushing injuries may easily develop septic shock.

6. Any major trauma depresses immunity and predisposes the animal to sepsis6.


1. In extensively bitten animals the clinician should rapidly assess the patient's mental status, mucous membrane colour, and capillary refilling time for symptoms of hypovolaemic and/or septic shock. Arterial pulse should be checked. When in shock, the pressure is down and the pulse weak.

2. A full rapid clinical examination should follow, with special attention to life-threatening problems e.g. patency of the upper airways, haemorrhage, open pneumothorax, and penetrating abdominal puncture wounds.

3. It is essential that the practitioner establishes early on in the course of treating a bite wound victim, the extent and nature of the injuries. In this way he can effectively plan the most appropriate way of dealing with each specific case.

4. The hair in the area of the bites should be atraumatically and extensively clipped (as described later). This will aid the practitioner in assessing the extent of the bites.

5. In all cases survey radiographs are mandatory as they are useful to indicate the extent of the damage (presence of air within the tissue planes), as well as indications of specific damage like fractures, pneumothorax and pneumomediastinum, pneumoperitoneum and peritoneal effusions.

6. A sterile blunt probe may be aseptically employed once the skin has been prepared (see later) to ascertain the extent of the wounds.



(1) Extensively bitten animals require intensive therapy, and owners should be cautioned that this kind of treatment is often prolonged and expensive.

(2) Shocked animals should receive appropriate intravenous fluid therapy at appropriate doses and rates. In addition, extensively bitten patients where substantial tissue necrosis and sepsis is anticipated require ongoing fluid therapy.

(3) These patients should be carefully monitored and nursed during the critical first few (5 to 7) days, especially with regard to cardiovascular and renal function. Urine output is a means of assessing overall perfusion of the tissues, particularly the kidneys6. Oliguria in shock is often due to inadequate fluid therapy6.

(4) Emergency surgery is rarely required in bite wound patients. The exception is penetrating abdominal punctures. Immediate surgical intervention and exploration is recommended for all penetrating abdominal bite wounds1 2. Attention should always be directed to life-threatening problems and an explorative laparotomy to assess the integrity of the gastrointestinal tract and other viscera as soon as possible after the patient has been stabilized may prevent the occurrence of serious peritonitis.

Generally, thoracic surgery is contra-indicated in cases of chest trauma, with the exception of unrelenting bleeding. In cases of open pneumothorax, the chest wall opening should be temporarily closed using a petrolatum-impregnated swab held in position with a light elastic dressing. Definitive closure can occur later when the animal has stabilized and the pneumothorax resolved. A chest drain may be necessary to correct the respiratory distress caused by pneumothorax if there is a penetrating thoracic wound8.

(5) Systemic antibiotics:

Prophylactic antibiotics, to be effective, must reach therapeutic concentrations at the site of the injury within three hours of contamination9. They must also be effective against the organisms contaminating the wound. No antimicrobial agent has been found to inhibit consistently the growth of the wide variety of organisms found in dog bite wounds5. For these reasons, antibiotics given to a bite wound victim at the time of admission, without any additional wound treatment, may only limit the spread of infection and the development of a bacteraemia, but they are unlikely to prevent local wound infection4. Simple wound lavage, surgical debridement of dead tissue and foreign bodies, combined with adequate drainage, are far more important in limiting local infection, than the administration of antibiotics3 4 5 8.

The drug selection should be effective against bacteria that would be expected in superficial wounds of dogs and cats; e.g. Staphylococci, Streptococci, E coli, and especially Pasteurella spp.8. Drugs with chemoprophylactic efficacy include ampicillin, amoxycillin, cloxacillin, cephalosporins, and clindamycin8. Metronidazole is found to be effective against most anaerobic bacteria. This spectrum may be expanded by the addition of enrofloxacin (Baytril, Bayer). When therapeutic antibiotics are used for an established soft tissue infection, they should be used for at least seven days8.

Evaluate deep and potentially serious wounds for antimicrobial therapy by taking swabs for bacterial culture and sensitivity tests (antibiograms) especially in chronic cases not responding to current therapy where resistance is suspected3 8.

(6) The caloric requirements of traumatized and infected animals markedly exceeds basal metabolic requirements. High energy foods with good quality protein should be fed to these patients. If animals refuse to eat, a nasogastric or gastrostomy intubation ,and a liquid diet is mandatory.

(7) Pain control:

Bite wound victims invariably experience severe pain and this should be addressed, with e.g. morphine or buprenorphine (Temgesic, R & C).


(1) PREVENTION OF FURTHER WOUND CONTAMINATION (aseptic technique, skin preparation, dressing).

Work aseptically with surgical mask and gloves in induction room or as prescribed in the sterile theatre.

The goal of proper wound hygiene is to provide a good environment for wound healing. Protect an open wound during preparation of the surrounding area by packing it with sterile saline or Ringer lactate moistened gauze sponges and fill the cavity with a water-soluble gel like K-Y jellyTM, (Johnson & Johnson)8. An eye ointment should be instilled into the conjunctival sacs to protect the cornea and conjunctiva when an area around the eye has to be prepared. Hair at the wound edges should be extensively trimmed with scissors or with a razor blade8. Hair must be shaved away from the wound to prevent it from dropping into the wound. An wide area around the wound should be clipped with an electric Oster clipper and No. 40 blade; this will permit inspection of the skin and evaluation of the extent of the injuries. Clip and shave the area around the wound. Surrounding skin should be washed with Hibiscrub (ICI) to reduce cutaneous bacterial load.

After the original gauze sponges or K-Y gel has been removed, the bite wounds should be flushed with luke warm tap water. Acriflavine in glycerine solution (Acriflavine in Glycerine KyronTM, Kyron Laboratories) can be applied into the wounds as an alternative if proper irrigation is not possible, because it promotes wound drainage and has a hygroscopic action which may reduce local swelling when applied with well-padded bandages or stents. The wounds are left unsutured to provide adequate drainage. Daily bandage changes are required, usually for the first 5 to 8 days. The use of an acriflavine glycerine compound in the management of contaminated and infected wounds stood the test of time in general veterinary practice over more than the last five decades. Acriflavine in glycerine enhances wound drainage due to its hygroscopic hypertonic action.

Due to the non-existence of scientific publications on the subject, a structured investigation has been initiated by a member of the Department of Surgery, to validate unpublished claims of effective wound care with acriflavin and glycerine.

Silver sulphadiazine cream on clean dry gauze can also be applied to the wound as a wet-to-dry dressing. It is also kept in place with well-padded protective bandages. Daily bandage changes is indicated for the first 4 to 5 days as necessary, according to the amount of wound drainage. Thereafter bandage changes can be done every second or third day until a healthy granulation tissue bed has formed.



(2.2) Puncture wounds should be surgically connected or widened.

(2.3) Passive drains in deep penetrating wounds.

(2.4) Secondary closure after debridement.

Secondary closure of an open wound is performed when a healthy bed of granulation tissue has formed. An incision is made around the wound at the junction of the epithelial tissue with the skin. Any epithelial tissue covering the edge of the granulation tissue should be removed. The skin around the wound is then undermined, and the skin edges are advanced across the granulation bed and sutured.

Some wounds are allowed to heal completely by granulating, contraction and epithelialization (second-intention healing), preferably covered with a stable bandage. Open wounds provide the optimum in wound drainage, but the time required for large wounds to heal may be prolonged. Dressings, bandages and hospitalization are expensive, but patients with open wounds need meticulous aftercare. Large wounds on the limbs and near joints may result in contracture and deformity requiring reconstructive surgery at a later stage.



(3.1) Surgical debridement:

The aim of wound debridement is the removal of infected and/or necrotic tissue. Surgical debridement is the most rapidly effective way of doing this, however, may not be entirely possible in extensively cases or where the wounds are in close proximity to vital structures (e.g. deep neck wounds). Surgical debridement should be performed as soon as the patient is stable enough to tolerate a general anaesthetic. Care should be taken to preserve intact blood and nerve supply to the remaining tissue. All visible devitalized tissue, especially fat and muscle, should be removed from the wound, leaving viable and questionable tissue3. Staged debridement may be used in some instances. During debridement, the wound should be lavaged with copious quantities of luke warm tap water or a lavage solution until all foreign material and dirt is removed from the wound. A flexible shower head connected to the water supply with the water coming out in a gentle (low-pressure) irrigating stream, works very well. It is preferable to lie the patient on a grid over a tub to allow the animal to stay dry and to avoid hypothermia in small patients. Detergents are deleterious to tissues, and therefore should not be used in cleansing wounds3.

The wound is covered with a clean gauze soaked in acriflavine glycerine (1:1000) to form a wet-to-wet dressing and bandaged. The well-padded bandage should be changed daily for the first 4 to 6 days. Any tissue that has changed from questionable to obviously necrotic is removed.

(3.2) Irrigation or lavage.

Wound lavage requires copious amounts of warm (20 - 25° C) fluid at a pressure of 1 - 2 psi (6,9 - 13,8 kPa)10. The effect is to remove debris, loose necrotic tissue and reduce the bacterial numbers by means of the washing action. Recommended fluids include municipal tap water, Ringer lactate solution and a 0,05% Chlorhexidine-diacetate (HibitaneTM, ICI) antiseptic solution (1:40 dilution of stock chlorhexidine in water) can reduce bacterial population9. (According to Swaim & Henderson (1990)3 dilutions of 0,1% to 0,5% Chlorhexidine tend to slow the development of granulation tissue.) Chlorhexidine acts quickly and has a sustained residual action, is not absorbed systemically and inactivation by organic matter does not seem to be disadvantageous, although some gram-negative bacteria appear to be highly resistant to its antimicrobial properties3. Chlorhexidine-diacetate should be diluted in sterile water, as a precipitate forms with saline.

A 20 ml syringe and 18 gauge needle attached to a sterile Ringer lactate container with a three-way stop cock may be used to irrigate the deeper aspects of the wound3 8. Irrigants should be delivered at a pressure of 8 psi to be optimally effective9. An improvised grid over a tub may be used to keep the rest of the animal dry while the wound is irrigated.


(3.3) Enzymatic debridement.

Enzymatic debridement is not a substitute for surgical debridement in the presence of a significant amount of necrotic tissue.8. Enzymatic debridement after thorough wound cleansing and irrigation may be used in severely injured patients in which the anaesthetic risk for proper surgical debridement is too great. It is also useful to apply in wounds affecting the distal extremities, where surgical debridement may inadvertently damage blood vessels, tendons, and nerves3 8. A variety of enzymatic debriding agents in aerosol sprays are currently available for use in the form of trypsin, with Balsam of Peru in castor oil base (DebrizymeTM, Kyron) and (VelzymeTM, Centaur). Antiseptic ointments or topical antibiotics may diminish the action of enzymatic debriding agents and should not be used concomitantly8. Two applications daily for 2 to 3 days, is usually sufficient.


All cases should be thoroughly examined physically, as injuries to underlying structures are often not seen. The systemic effects of severe multiple trauma as a result of extensive tissue necrosis and infection needs to be considered when treating these cases. Systemic management with the aid of intravenous fluids, antibiotics, and pain control is of prime importance.

The extent of puncture wounds of the chest and abdomen should be carefully examined with the aid of sterile probing to determine their depth, and also by radiographic and ultrasonic evaluation of the viscera for any signs of perforation or effusions.

Local wound management

- pack wound with sterile KY jelly to prevent further contamination when cleaning

- clip surrounding hair and wash the skin with surgical scrub (HibiscrubTM, ICI) extensively.

- lavage with large quantities of municipal tap water under gentle pressure, or 0,05% chlorhexidine (HibitaneTM, ICI) in sterile water, or Ringer lactate in 20 ml syringe and 18G needle

- silver sulphadiazine wound dressing (Argent-EzeTM, Lennon) or (FlamazineTM, Lennon) on Jelonet or clean gauze swabs

- alternatively, acriflavine in glycerin (Acriflavine in Glycerin KyronTM, Kyron Labs.) may be used onto the wounds and covered by clean gauze swabs

- well-padded bandage to keep wound dressings in position, prevent further contamination and absorb exudate

- lavage wounds and change wound dressings and bandages daily

Use of antibiotics

Broad spectrum antibiotics should be given within 3 hours after the biting injury to be effective, otherwise it is only given to suppress local spreading of infection or bacteraemia development.

Systemic antimicrobials active against aerobic and anaerobic bacteria are combinations of:

Synulox + metronidazole

amoxycillin + metronidazole

Bacterial cultures and sensitivity testing should be considered in debilitated patients and deep penetrating wounds or contamination of body cavities.


Routine primary closure of bite wounds is contra-indicated

Primary closure after meticulous surgical debridement however is indicated in the following:

facial wounds with functional impairment eg lacerated lip/eyelid

wounds penetrating body cavities


Fresh lacerated bite wounds

Broad spectrum antibiotic (aerobic + anaerobic bacteria)

Wound hygiene (clip hair + shave surrounding skin)

Thorough lavage of the wound (municipal tap water, or 0,05% chlorhexidine in water, or Ringer lactate with 20 ml syringe + 18G needle)

silver sulphadiazine dressing under bandage, or acriflavin in glycerine 1:1000 liquid into wound + cover with a well-padded bandage

Open wound healing - after 3 - 5 days - delayed primary closure + Penrose drain(s)

minimal necrotic tissue -

Meticulous surgical layer debridement of all contaminated tissues, after 3 - 5 days - delayed primary closure + penrose drain(s)

necrotic tissue/infection - local wound management + surgical debridement

secondary closure (after 5 days) OR

second intention healing

Fresh puncture wounds

Broad spectrum antibiotic (aerobes + anaerobes)

Wound hygiene (clip + shave hair around wound)

Lavage / irrigate as thoroughly as possible

Leave wounds unsutured with silver sulphadiazine dressings and well-padded bandage, or alternatively, apply acriflavine in glycerine 1:1000 onto wound (with or without drains)

Remove scabs daily for first 2 - 3 days to allow adequate drainage

Leave to heal as open wounds (secondary union) preferably under a well-padded bandage

Neglected / infected bite wounds

Swabs for bacterial culture + sensitivity tests

Specific antibiotics (aerobes + anaerobes)

Wound hygiene

Thorough lavage of the wound

Surgical debridement of necrotic + infected tissues (layer or en bloc debridement)

Silver sulphadiazine dressing under a well-padded bandage, or, alternatively, apply acriflavine in glycerine 1:1000 dressing + bandage

Large wounds - secondary closure (after 5 days or longer)

Small wounds - second intention healing.


1. Neal TM, Key JC. Principles of treatment of dog bite wounds. Journal of the American Animal Hospital Association 1976; 12(5):657 - 660

2. Fleisher GR, Boenning DA. The treatment of animal bites in humans. The Compendium on Continuing Education for the Practicing Veterinarian 1881;3(4):366 - 370

3. Swaim SF, Henderson RA. Small Animal Wound Management. Lea & Febiger, Philadelphia, 1990:9 - 51, 69 - 72

4. Cowell AK, Penwick RC. Dog bite wounds: A study of 93 cases. The Compendium on Continuing Education for the Practicing Veterinarian 1989;11(3):313 - 320

5. Goldstein EJC. Management of human and animal bite wounds. Journal of the American Academy of Dermatology 1989;21(6):1275 - 1279

6. Hauptman J, Chandry IH. Shock, In: Disease mechanisms in small animal surgery, second edn., Bojrab MJ, Smeak DD, Bloomberg MS (eds.) Lea & Febiger, Philadelphia, 1993: 17 - 20

7. Schultz RD. The effects of aging on the immune system. The Compendium on Continuing Education for the Practicing Veterinarian 1984;6(12):1096 - 1105

8. Bright RM, Probst CW. Management of superficial skin wounds, in: Textbook of Small Animal Surgery, Slatter DH (ed.) WB Saunders Co., Philadelphia 1985:431 -443

9. Riviere JE, Kaufmann GM, Bright RM. Prophylactic use of systemic antimicrobial drugs in surgery. The Compendium on Continuing Education for the Practicing Veterinarian 1981;3(4):345 - 354

10. Swaim SF. A "walking" suture technique for closure of large skin defects in the dog and cat. Journal of the American Animal Hospital Association 1976;12(4):597 - 599

11. Kirby R. Systemic inflammatory response syndrome: How to keap them alive! Proceedings of W.S.A.V.A. XIX World Congress, Durban 1994:186-194

These guidelines for bite wound management in dogs and cats was compiled and is currently (December 1996) in use by the surgeons in the Small Animal Section, Department of Surgery, University of Pretoria, Faculty of Veterinary Science, Onderstepoort.


Prof G L Coetzee - Acting Head of Small Animal Section

Prof A M Lübbe

Dr N Lambrechts

Dr M Booth

(Published -December 1996)

Euthanasia in Adult Non feral Cats and Dogs

Intra-peritoneal injection is the second method of choice on the following grounds:

The absorption of drugs placed into the peritoneal cavity may be erratic.  Clinically, this means that the intake of euthanasia agents may be slow and prolonged.  All euthanasia agents currently available in South Africa are barbiturate based.  With slow absorption of the anaesthetic agent, the phases of voluntary excitement may be seen after intra-peritoneal injection.   The excitatory effects are seldom seen.  It is advised in United States protocols for intra-peritoneal euthanasia to place the patient in a quiet environment during this phase to avoid unnecessary excitement.  Sedative drugs will also reduce the incidence of excitation.  Erratic absorption may be partial overcome by increasing the dose of the euthanasia agent given intra-peritoneal.  No specific dose is currently available but guides recommend at least doubling the dose;

Should injection of the euthanasia agent occur in the loops of the gastro-intestinal tract, euthanasia is unlikely to be achieved.  Rupture and damage to abdominal organs are potential complications.  Meticulous attention to the techniques of intra-peritoneal injection needs to be paid;

Delayed absorption of drugs may lead to unnecessary suffering of patient.  This may be of particular importance in patients in shock;

Intra-peritoneal injection of barbiturates is irritant to the peritoneum.  Clinically, pain on injection with pentobarbitone is usually not seen.  Intra-peritoneal administration of barbiturates for anaesthesia is only recommended for non-recovery surgery due to the peritonitis that forms.  As a method of euthanasia, the peritonitis induced, per se, is not problematic; and

The intra-hepatic injection of euthanasia agent is controversial and not recommended.


Intravenous injection is the first method of choice;

Intra-peritoneal injection is the second method of choice.  This route is acceptable as a first choice in rodents, reptiles and small birds.  This route is also appropriate if an intravenous injection is not possible e.g. aggressive patients, limited experience with intra-venous injection techniques;

Intra-cardiac injection should only be performed on heavily sedated or anaesthetised patients as a last resort;

Animal Welfare Assistants should be trained with regard to the technique, pharmacology of intra-peritoneal injection and the safe handling of these drugs; and

Difficult patients may be better euthanased, after induction of anaesthesia through a suitable intra-muscular anaesthetic protocol.

(Published- August 2000, courtesy of Dr K E Joubert)




Etorphine is a semi-synthetic opioid, derived from morphine.  It has a potency 10 000 times that of morphine sulphate.

Opioids are more commonly known as narcotic analgesics, which apart from their analgesic effect have a wide range of other pharmacological effects including antitussive, antidiarrheal, emetic and psychotropic effects.

Marked respiratory depression and addiction are very important adverse effects associated with the opioids.

Large species differences occur, particularly in the psychotropic effects of opioids, which vary from excessive stimulation to marked depression of the central nervous system.

The potent narcotic anaesthetic effect of etorphine has led to its extensive use as a chemical immobilisation agent in game.

The availability of an antagonist has further promoted the safe use of etorphine in game.

Etorphine is legally only available for use under veterinary control.

The requirements for control and conditions of use of etorphine are strictly governed in terms of the Medicines Control Act (Act 101/65) and the Veterinary and Paraveterinary Professions Act (Act 19/82), respectively.  These are outlined for each Act.


Medicine   Act 101/65                                                                 Veterinary Act 19/82

↓                                                                                                ↓

Control                                                                                       Use



The Medicines Control Act (Act 101/65) provides for the availability and requirements for control of medicines in South Africa.

Medicines become available following registration in terms of the requirements of the Act or under exceptional circumstances by provision of a permit under Section 21 of the Act.

Supply and use of medicines are controlled in terms of the schedule requirements of medicinal substances as described in Section 22A of the Act.

Prescription, dispensing and register requirements for the supply and use of medicines are described in the Regulations of the Act.

Schedule requirements of etorphine

Schedule 7 substance*

Etorphine, like other opioids, is classified as a Schedule 7 substance due to its undesirable dependency

Prescription only medicine

Etorphine can be supplied or used on the prescription of a veterinarian. Only a veterinarian is entitled to issue a prescription for etorphine.

Prescription access

Veterinarians and pharmacists have free access to etorphine whereas para-veterinary persons may only have access in the presence of a veterinarian or through a prescription.

Scope of use

A scheduled substance can only be prescribed by a veterinarian in his/her normal scope of practice.


Schedule 7 substances are controlled according to the international convention on narcotic substances to which South Africa is a signatory. Each country receives an annual quota.

Prescription requirements


A prescription can only be issued for a specific patient, therefore a prescription for etorphine cannot be issued to a game capturer when the patient is not under control of a veterinarian. A patient could refer to a group of animals. A person in possession of a schedule 7 substance must be in the possession of a valid prescription. Please note that this guideline is no longer in place as the  Veterinarian must be the end user of chemical restraint and capture of animals.


The contents of a prescription are described in the regulations. In the case of a schedule 7 substance, such as etorphine, the amount prescribed must be written in both letters and words.

Time valid

A prescription for a schedule 7 substance is only valid for 30 days and may not be repeated.

Amount permitted

Not more than 30 days’ supply of a schedule 7 substance may be prescribed for a patient.

Contents of a prescription


Name and address of veterinarian or practice

Name and address of owner

Identification of animal(s)

Name and quantity of medicine

Dosage form

Volume or mass of dosage form

Age or group of animals

Complete instructions for use

Signature and qualification of veterinarian

Dispensing requirements


A schedule 7 substance can only be supplied on prescription. A patient card can serve as a prescription book provided the details recorded are in compliance with those of a prescription.


All medicines supplied by a veterinarian must be labelled in accordance with the regulations.


All records of the sale and use of etorphine must be kept for a period of 5 years and must be readily retrievable.


Schedule 7 substances must be kept under lock and key. Only veterinarian(s) in the practice may have access to the key.


Disposal of schedule 7 substances must occur in the presence of an inspector of the Medicines Control Directorate or any person appointed by the MCC.

Label requirements

Name of medicine or of each active ingredient or constituent. (Must state "Non nomen proprium" If veterinarian wishes not to state this information)

Name of client and brief description of animal(s)

Directions for use

Name and address of veterinarian or practice

Warning regarding withdrawal period (if applicable)

Maintenance of register

S7 Register

Every sale of a schedule 7 substance must be recorded in a "Schedule 7 register".


Date of receipt or sale; name, business address and invoice or reference number of supplier and in case of import, the import number; name and address of client to whom substance was sold; and quantity of substance received or sold, indicated per dose unit, mass or volume

Balancing of register

The register must be balanced for each schedule 7 substance remaining in stock on the last day of March, June, September and December of every year.


The senior partner in the practice is responsible to ensure that the register is maintained.


The Veterinary and Para-veterinary Professions Act (Act 19/82) describes the scope of practice of a veterinarian which involves the supplying and selling of any veterinary medicine and rendering of a veterinary service.

The requirements for sale and the conditions of use of medicines by veterinarians are specified within the rules of the Act



The diagnosis, treatment and immobilisation/anaesthesia of wild animals remains the responsibility of the veterinarian.  The Veterinarian is the end user of scheduled substances.


The chemical immobilisation/anaesthesia of wild animals by non-veterinarians is not acceptable and should not be undertaken.  Only a wildlife veterinarian qualified and who belong to a professional organisation under the control of the Veterinary Council may chemically immobilise anaesthetise animals.


The Veterinary Council may, after consideration of an application by a person not registered in terms of Act 19/82, authorise him/her to render for gain such services as deemed to pertain to those of a veterinarian or paraveterinary profession subject to conditions as determined by Council.

Justification for use of medicinal products

In terms of the rules of the Veterinary Council a veterinarian must be satisfied that the administration of a drug is justified after consideration of the risk-benefit that is associated with its use. This should include consideration of:

Animal(s) which will receive treatment

Consumer of animal products

Client Information

The following drug information needs to be conveyed to clients when supplying any medicine

Route and site of administration


Drug effects including adverse reactions

Precautions which should be taken into account

Withdrawal period where applicable

Dispensing responsibilities

The following factors should be considered when dispensing any veterinary product:

Competency of the client or user of drug/ only the veterinarian may use this drug

Must be a bona fide client. No open shop allowed.

Necessity of permanent record of all sales (5yrs)

Compliance with all schedule requirements


The legal use of etorphine for the immobilisation of game is subject to both the requirements for control in terms of Act 101/65 and the conditions of use under Act 19/82

Act 101/65 permits the use of etorphine under prescription of a veterinarian provided there is compliance with the scheduling, prescription, dispensing and register requirements of the Act.  The use of etorphine is limited to registered trained veterinarians.

Act 19/82 describes the conditions of use of medicinal products in animals and restricts certain procedures to veterinarians

The responsible use of etorphine is also in the interest of the public


Legal requirements for the use of Etorphine in game

Note that in terms of the new regulations of Act 101, Schedule 7 substances will be reclassified as Schedule 6.

(Published- December 2001, courtesy of Prof G E Swan) Amendments to the advise 2006 /07


Diagnosis Feline Infectious Peritonitis (FIP) – more than just a titre.

Dr Liesel L. van der Merwe,  Department of Companion Animal Clinical Studies, Section of Small Animal Medicine

Faculty of Veterinary Science, University of Pretoria .  Edited by Dr Alain Carter and Dr Heidi Schroeder.

Feline infectious peritonitis (FIP) is caused by the feline corona virus (FCoV) which also causes a common, usually subclinical, viral diarrhoea in cats. The virus causing FIP is a mutation of the feline enteric corona virus (FCoV). There is no FIP virus. The same virus is responsible for both diseases. It was initially hypothesised that the enteric corona virus and FIP causing strains were different – but they are serologically and genetically indistinguishable.

FcoV is shed mainly in the faeces. In early infection it may be found in urine and respiratory secretions. The transmission is by faecal-oral route and the virus infects the intestinal epithelium. All felidae are affected. Although relatively fragile FCoV can survive for up to 7 weeks in dry conditions. Indirect fomite transmission is thus possible. Is sensitive to most household detergents and disinfectants. Endemic infection is maintained by continuous re-infection via the litterbox. Many naturally infected healthy cats will shed virus intermittently for up to 10months. About 20% will become chronic shedders. Cats with high antibody titres are more likely to shed virus at higher levels and more consistently. Most cats with FIP will also shed FCoV (non mutated), the amount of virus shed declines as the disease progresses.

Mutated FIP has not been found in secretions or excretions of cats with FIP, thus natural transmission of mutated virus is unlikely, although iatrogenic transmission is possible, for example with surgery via instruments.

Increased incidence of FIP occurs with indoor cats, litter boxes and multi-cat households as crowded environments increase stress and exposure to FCoV.

Cats are at the greatest risk of developing FIP in the first 6-18 months after infection with FCoV and the risk decreases to 4% 36 months after exposure.

Susceptibility in young cats is increased because of undeveloped immune systems and stressors such as vaccination, re-homing and neutering.

FCoV is subject to frequent RNA mutations. Certain of these mutations allow the virus to enter and replicate within feline macrophages. These macrophages are part of the alimentary immune system and lie under the intestinal epithelium.

Once the virus has entered the macrophage it is the cats’ immune reaction which determines what, if any type of disease will develop.

·         Cats which have a well developed immunity and mount a good humoral and good cell mediated immune response will not develop FIP.

·         Cats developing a good humoral but only a partial cell mediated immune response will develop the granulomatous/dry form of FIP. In cats with a partial immune response the disease will often present once the cat is a young adult. The disease mechanism in these cases is a pyogranulomatous perivascular reaction.

·         In cats which have a poor cell mediated immunity and only develop humoral immunity, the wet / effusive form will develop. Younger cats which are exposed to mutated forms of FCoV are more likely to develop the wet form. These cases will also develop clinical signs earlier on in the course of the disease. The underlying pathophysiology of the wet form is an immune mediated vasculitis resulting in increased vascular permeability and the effusion of a protein-rich fluid.

Viraemia occurs both with the enteric and mutated form of the virus. The viraemia with the enteric form is however short-lived and low grade. Up to 80% of cats can be viraemic in affected multi-cat households. Corona virus antibodies are present in 90% of cats in catteries and up to 50% of cats in single cat households. Only approximately 5% of FCoV infected cats will develop FIP in a cattery.


Ante-mortem diagnosis is difficult as there are no specific clinical signs, a lack of specific haematological and biochemical abnormalities and the tests routinely used in practice have a low sensitivity and specificity. A presumptive diagnosis will depend on a combination of findings.

1.             Clinical Presentation

Signalment: The peak age distribution is 6 months  - 3 years although any age can present. There is no breed or sex predilection. Most patients will have originated from multi-cat households, specifically greater than 5 cats. These cats will often have a history of failure to thrive.

Studies have shown that sexually intact and purebred cats, males and young cats are more likely to be diagnosed with FIP, all of these factors are likely due to crowded kennel situations.

2.             Physical examination

FIP will present as an effusive wet form or as the granulomatous dry form. Young kittens may present prior to the development of noticeable effusions. Younger cats will more likely present with the wet form, and older cats with the dry form.

Common presenting clinical signs include: a cyclical, antibiotic unresponsive, fever, lethargy and icterus.

In the wet form, fluid effusions result in ascites, sometimes with scrotal accumulation, pleural effusion and a pericardial effusion. This fluid is a yellow tinged, protein-rich, inflammatory, sterile exudate.

The dry form may present with abdominal masses (often affecting the liver, kidney, spleen and mesenteric lymphnodes) and neurological signs. Ocular FIP presents with keratitic precipitates, anterior uveitis, hypopyon and hyphema. Irregular kidneys, enlarged mesenteric lymphnodes and thickening of the intestines, especially at the ileocolic junction may be palpated.

3.             Clinical Pathology

3.1   Haematology and biochemistry

Haematology and clinical chemistry are non-specific. A mild anaemia, due to chronic inflammatory disease, a mild neutrophilia and a lymphopaenia (< 1.5 x 109) often occur. Hyperproteinaemia, typically a TSP  > 80 g/L is common and is caused by hyperglobulinaemia. The likelihood of FIP is 90% with globulins >120g/l. A serum A:G ratio of < 0.8 has a 92% positive predictive value and a 61%  negative predictive value if >0.8. Other chemistry results include hyperbilirubinaemia, which is common and due to vasculitis within the liver. Affected cats can have severe liver disease and may present with increased liver enzymes and coagulopathies. Grouped clinical pathology abnormalities increase the predictive value: Lymphopaenia , hyperglobilinaemia and an antibody titre > 1:160  have a PPV 88.9% and NPV of 98.8%.

3.2   Effusion Examination

The fluid is an exudate with an SG > 1.017, > 35g/L protein and moderate numbers of non-degenerative neutrophils, macrophages and lymphocytes. Less frequently the fluid may be identified as a modified transudate. Bacteria may be present in the fluid and are an indication of severely decreased immune resistance. A total protein content >35g/l with globulins accounting for ≥ 50% had a positive predictive value of 94% and a negative predictive value of 100%. Abdominal ultrasound examination may facilitate the detection and sampling of small fluid accumulations in earlier cases.

3.3   Cerebrospinal fluid (CSF) evaluation

Cats with neurological FIP are generally serologically positive in the CSF as well as serum positive. Ratio of CSF antibody to serum antibody is higher than that of CSF protein to serum protein

4.             Serology Tests

Recap of Important facts:

The virus causing FIP is a mutation of the FCoV but is serologically and genetically indistinguishable. This means that both antibody titres as well as PCR techniques will be non-specific.
Viraemia occurs both with the enteric and mutated form of the virus. Up to 80% of cats can be viraemic in affected multi-cat households.
Corona virus antibodies are present in 90% of cats in catteries and up to 50% of cats in single cat households. Only approximately 5% of FCoV infected cats will develop FIP in a cattery situation.


Titres do NOT differentiate between FCoV producing diarrhoea and FIP.
Paired rising titres could reflect FIP or FECV
The titre increase is NOT correlated to the severity of disease.
The titre is not indicative of active disease

Serology has been shown to have a positive predictive value for FIP of only 38.9%.

Serological tests for titres include IFA and ELISA testing. Dilutions should start at 1:25

If the result is negative, the following interpretations apply; truly negative, very recent infection (< 10 days), Immune complex consumption of free antibodies, acute fulminant disease. Titres > 16000 are generally indicative of FIP.

5.             Reverse Transcriptase Polymerase Chain Reaction (RT-PCR)

RT -PCR tests for antigen in tissue. Blood, tissue and effusions can be used. Due to the numerous sites of mutation of the FCoV it is impossible to make a FIP mutation specific primer. The PCR test thus tests for FCoV, and also cross reacts with canine corona virus (CCV) and transmissible gastroenteric virus (TGEV). False negative results may occur due to insufficient infected cells (macrophages) being present in the material. Occurs with especially CSF.

RT –PCR is very sensitive to detect virus shed in faeces. And the strength of the reaction is correlated to amount of virus in the faeces. The test should be performed daily for 4-5 days as shedding can be intermittent. Cats shedding for > 6 weeks are classed as continuous shedders.

6.             Histopathology

Histopathology is the only diagnostic test able to confirm a diagnosis of FIP and coeliotomy with biopsies of abdominal organs should be offered as an option to the client. H&E stained smears show localised perivascular inflammatory reaction with macrophages, neutrophils, lymphocytes and plasma cells. Pyogranulomas range from microscopic to fairly large. PCR as well as immunocytochemistry may be performed on formalin fixed biopsies.


There is no effective treatment. Various immunosuppressant drugs have been tried and may prolong progression for a short period, but all cats will die from the disease.


Prevention is the goal.

1)                   Preventing FIP for in contact cats

2)                   Prevention of FIP in cats with FCoV

3)                   Preventing FCoV

1) In case of a positive diagnosis with FIP in a household / cattery, full siblings have a 0.25 – 0.5 probability of dying from FIP, otherwise the risk is no greater for other cats getting FIP than in any other cat households which are positive for FECV.

2)                   FCoV is endemic in all  > 5 multi-cat households. There is no way specifically to prevent mutation. Management tools include: Support natural resistance and decrease stressors

Reduce FCoV challenge

§         Decrease number of kittens < 12 months old

§         Cleanliness

§         Encourage use of outside garden for toileting

§         Do not breed from queens that show repeated litters affected with FIP  - select for resistance.

§         Decrease cat numbers to < 5

§         40-60% cats shed intermittently FCoV

§         20% of cats will be persistent shedders FCoV

§         20% immune and will not shed FCoV

Repeated faecal PCR examination should be performed weekly for up to 2 months to check for shedding. Remove persistent shedders. Early weaning is a suggested means to decrease transmission but transmission can occur from 5 weeks and this is too early to wean kittens, this it is not a very feasible option.

2)                   Fomite transfer of FCoV

The virus is easily transmitted and survives for up to 7 weeks in dry conditions. It is sensitive to most disinfectants and household detergents so general cleanliness is important.


1.        An Appraisal of the Value of Laboratory Tests in the Diagnosis of Feline Infectious Peritonitis. Sparkes, A.H. Gruffydd-Jones, T.J. and Harbour, D.A. Journal of the American Animal Hospital Association. 1994 (3) pg 345 – 350

2.        Clinical assessment of the diagnostic value of feline alpha-1-acid glycoprotein for feline infectious peritonitis using the likelihood ratios approach. Saverio,P. et al Journal of Veterinary Diagnostic Investigation 2007 (3) pg 266 –272

3.        Feline Infectious Peritonitis. Hartmann, K. Veterinary Clinics of North America . 2005 (35) pg 39 – 79

4.        Infectious Diseases of the Dog and Cat. Ed. Craig E Greene. 3rd edition. Published by Saunders Elsevier


General concepts of sensitivity and specificity:

Sensitive test correctly places all affected animals in the positive category (prone to false positives)

Specific test correctly places all unaffected animal in the negative group (prone to false negatives).

All tests have a calculated sensitivity and specificity based on certain cut-off levels in order to maximise either sensitivity or specificity at the expense of the other.

The prevalence of a disease in a test population profoundly influences the accuracy of a test result  so only selected patients should be tested– i.e. typical clinical signs etc.

The predictive value indicates how accurately a test result will predict the infection status of an individual in a target population.

The predictive value of a negative test is much more resistant to changes in disease prevalence

TABLE 1: Methods to assist in diagnosing FIP antemortally

Clinical Presentation

Clinical Sign


Other differentials


50% of cats with effusion actually have FIP

(30% with thoracic effusion, 60% of cats with ascites only, 30% of cats with both).


Lymphoma, Pyothorax, heartfailure, chylothorax, trauma, lung lobe torsion, diaphragmatic hernia.

Ocular Changes

Retinal changes – cuffing of vasculature, haemorrhage, detachment, granulomas.

Uveitis – iris colour change, aqueous flare, keratitic precipitates.

Toxoplasmosis, systemic fungal infections, FIV, FeLV.

Neurological signs

13% of cats with FIP have neurological signs

17% of cats with neuro signs had FIP.

Clinical Pathology Changes




- Lymphopaenia

(< 1.5x109/l)

- Neutrophilia

- Anaemia

98% negative predictive value.


Hyperglobulinaemia:Hypergammaglobulinaemia may be polyclonal or monoclonal.

- Hypoalbuminaemia

Likelihood of FIP is 90% with globulins >120g/l

Serum A:G ratio < 0.8 is a 92% positive predictive value. Serum A:G>0.8 is a  61%  negative predictive value.

Alpha-1 acid glycoprotein.

> 1500mg/ml in effusion or serum occurs with FIP.

Increased in several infectious diseases in cats.


Modified transudate or exudates:

High protein content >35g/l

Low cellular content (<1000 nucleated cells / ml)

Pyogranulomoatous cytology: macrophages and neutrophils.

Lymphoma, heart failure, cholangiohepatitis, bacterial peritonitis or pleuritis.

Specific Diagnostic tests
Serology – antibodies

Serum Antibodies:

Tests for feline corona virus  - NOT FIP!

Many asymptomatic shedding cats have high and increasing titres.

Test method is important – need to quantify the antibody titre.

10% of cats with FIP have negative results (all bound)

Highest measurable titre  - (v high titres) increases likelihood of FIP. Positive predictive value of 94% in a suspect population.

Best application of antibodies is to exclude shedders, and clear up a cattery – the height of the titre is directly associated with viral enteric replication and therefore shedding.

Effusion Antibodies

Serological tests on effusion have higher diagnostic value than tests on blood.

Reports differ on efficacy.

FCoV antibodies in effusion have a 90% positive predictive value and a  79% negative predictive value.

CSF antibodies

Two reports – divided on efficacy.

Polymerase Chain Reactions (PCR)

PCR  - Blood

Non specific for FIP.

FCoV also causes transient viraemia (PCR positive in cats which did not develop clinical signs of FIP for 70 months).

PCR effusion

Insufficient data.

PCR in faeces

Sensitive to document shedding.

Should be performed daily for 4-5 days as shedding can be intermittent. Cats shedding for > 6 weeks are classed as continuous shedders.

Histopathology and immunohistochemistry

Antigen detection in effusions

IF staining to look for FCoV in macrophages.

100% positive predictive value but poor negative predictive value (57%) because false negatives can occur with insufficient cellular material.

Tissue Biopsy

H &E immunohistochemistry

100% identification of FIP.      Doesn’t distinguish between enteric and FIP form, but the enteric form shouldn’t be in macrophages.

(Published August 2008 -Courtesy Dr L L van der Merwe)

Links to African Council websites

Veterinary Statutory Bodies in Africa

Veterinary Council of Namibia

Veterinary Council of Zimbabwe (department of livestock and veterinary services)

Kenya Veterinary Board

Veterinary Council of Tanzania

Botswana Veterinary Association

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